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100 Cards in this Set

  • Front
  • Back
abrupt onset and termination
paroxsymal
SVT characteristics
paroxsymal
>180BPM
Pwave hidden in QRS
reg rhythm
normal QRS
origination of eptopic focus is above bifurcation of bHIS
SVT
causes of SVT in normal heart
overexertion
emotional stress
stimulants
dig tox
cor pulmonale
CAD
RHD
tx for SVT
vag maneuvers
adenosine
verapamil
cardioversion
when is direct cardioversion used for SVT
when vag maneuvers and drugs do not work
how is adenosine given
6 mg rapid followed with 20ml NS
what happens if no results after first dose of adenosine
give 12 mg rapid followed by bolus of NS
SE of adenosine
flushing
chest pain/tightness
brief asystole
bradycardia
PAC
atria firing early
contractions originating from ectopic focus in atrium from somewhere other than SA node
PAC
what causes PAC
waves travel across atria by abnormal pathway creating distorted p wave
rate of PAC
reg except where PAC is
causes of PAC
emotional stress
caffeine/tobacco/ETOH
hypoxia
drugs
electrolyte imbalances
COPD
valvular disease
when are PACs a concern
in ppl with heart disease d/t to possible sign of more serious dysrhythmia
tx for PAC
b-adrenergic blocker
diltiazem (cardizem)
propafenone (rhythmol)
amiodarone
flecanide (tambicor)
clonidine (catapres)
MG
recurring regular saw tooth shaped flutter waves
a flutter
what does a flutter cause
blood to pool in atria d/t weak contractions
a flutter characteristics
250-350bpm
from single ectopic focus
vent rate reg or irreg
QRS normal
concern for a flutter
hih vent rates and loss of atrial kick can decrease CO
serious risk with a fluter
stroke
causes of a flutter
atrial stretching
CAD
ETOH
pericarditis
HTN
mitral valver dis.
PE
chronic lung dis
cardiomyopathy
hyper thyroid
dig/ quinidine/epi
clinical sx of a flutter
palpitations
decreased CO
CHF
tx for a flutter
b adrenergic blockers
cardizem
rhythmol
amiodarone
flecinide
clonidine
drugs that slow HR
CCB
b adrenergic blockers
other tx for a flutter
cardioversion
radiofrequency catheter ablation
long term tx of choice for a flutter
ablation
results d/t multiple ectopic foci resulting in loss of atrial contraction
a fib
twitching of atria
a fib
charac of a fib
p wave not recognizable
cant measure PR
irregular
atrial rate > 350
causes of a fib
ETOH intox
cafffeine
electrolytes
cardiac surg
can result from a fib
thrombi
embolus
decrease CO
tx for a fib
decrease vent response
prevent embolic stroke
dig/ CCB/ BAB
heparin
coumadin (long term)
if pt is in a fib for >48hrs what is recommended b4 cardioversion
anticoag therapy with warfarin for 3-4 wks before and 4-6 wks after
other tx for a fib
radiofrequency ablation
maze procedure
contraction originating in ectopic focus of the vents
PVC
characteristics of PVC
wide and distorted QRS
a pause may follow
Pwave not visible
multifocal PVC
more than one place firing
unifocal PVC
one place firing with them looking similar
Q 3rd beat is PVC
trigeminy
q 2nd beat it PVC
bigeminy
why is pwave absent with PVC
not firing from sa node
tx for PVC
oxygen
electrolyte replacement
drugs
run of 3 or more PVC
vent tach
characteristics of vtach
150-250 bpm
monomorphic/polymorphic
sustained/unsustained
pulsatile/unpulsatile
why is there no pwave with v tach
rapid vent firing
causes of v tach
Mi
CAD
hypoxia
bradycardia
drugs
electrolyte imb
long Qt syndrome
dig tox
CNS disorders
tx for pulseless vtach
CPR
causes of v fib
acute mi
CAD
hyperkalemia
hypoxia
acidosis
drug toxicity
class 1
na channel blockers
what do the class 1 drugs slow
atria
vents
Bhis
class 1A drugs
quinidine
procainamide
disopyramide
what do the class 1A drugs do
widen QRS
prolong QT
reduce automaticity
prolong refrac. period
nsg imps for class 1 a
mtr cardiac rhythm
monitor bp
class 1b drugs
lidocaine
mexiletine
phenytoin
what do class 1 B drugs do
supress automaticityin
- Bhis
-fibers
-
class 1 a drugs do what
supress dysrhytmia
SE of class 1B
difficulty breathing/swallowing
convulsions
resp dep
neurotoxicity
cardiovascular collapse
nsg imp for class 1 B
mtr bp/ ecg cont.
resp and neuro status
mtr serum blood levels
when should 1B drugs be stopper
prolonged PR or QRS
new dysr
slows conduction velocity and increases vent refractoriness
class 1 C
class 1 C drugs
flecanide
propafenone
nsg imp for class 1 C
correct K levels before giving
mtr serum blood levels
action of class 2
block effects of epi
decrease SA automaticity
slow av conduction
slow myocardial contractility
drugs of class 2
propanolol
esmolol
acebutolol
SE of class 2
anaphylactic reaction
steven johnson syn
laryngospasm
bronchoconstriction
bradycardia
nsg imp for class 2
mtr VS before and after
mtr for hypotension
Class 3
K channel blockers
class 2
beta blockers
effect of class 3
prolong duration of action potential refrac period
txs life threat- vent dys, SVT
and a fib
SE of class 3
hypotension
dizziness
sinus arrest
class 3 drugs
amiodarone
bretylium
sotalol
ibutilide
dofetilifde
nsg imp for class 3
correct K and Mg before
mtr for hypotension
long half life
class 4
Ca channel blockers
drugs for class 4
verapamil
diltiazem
digitalis
adenosine
actions of class 4
reduce automaticity in SA
slow conduction in AV
SE of class 4
hypotension
av block
nsg imp for class 4
correct k and mg
mtr serum drug levels
junctional characteristics
originates in av node area
sa failed to fire or blocked at av
40-60bpm
may or may not have p wave
causes of junctional
cad
heart failure
cardiomayopathy
electrolyte imb
inferior mi
RHD
drugs
accelerated junctional
60-100
junctional tach
100-250
arrythimias frin delayed or failed conduction of supravent impulses to vents
av block
every impulse is conducted to the vents but duration of av conduction is prolonged
first degree
first degree charac
PR > .20
each p wave has qrs
pr interval is constant
causes of type 1 block
Mi
cad
rhd
hyperthy
vag stim
drugs
gradual lenghthening of PR and eventually qrs is dropped
second degree type 1
causes of second degree type 1
dig
BAB
CAD
pwave not conducted and pr stays the same
second degree type 2
causes of 2nd type 2
RHD
cad
anterior MI
dig tox
often progresses to 3 degree
2nd type 2
tx for 2nd type 2
pacemaker
has a vent escape
third degree
lacks t waves
3rd degree
tx for 2nd type 2
pacemaker
form of av dissociation in which no impulses from the atria are conducted to the vents
3rd degree
abnormal cardiac rhythms
dysrhythmias
output of defib measured in what
joules
360 joules
monophasic defib
150-200 joules
biphasic defib